Physiologic Optimization

Abram Feldman

Raquel R. Bartz

INTRODUCTION

Managing a patient’s airway requires considering the patient as a whole, even as securing the airway itself may be the most salient issue at that moment. In the ICU, respiratory failure requiring intubation has multiple causes, and the intensivist must consider the interactions between other organ systems and their impact on airway management when these situations arise. Optimizing a critically ill patient’s physiology prior to and during airway management can mean the difference between a safe transition to mechanical ventilation and a cardiac arrest.¹ The objective of mechanical ventilation is to provide the patient help with gas exchange, limit iatrogenic lung injury, and do so without undue stress on their cardiovascular system. Every one of these patients requires intubation in order to do so, regardless of how, or how severe, their physiology became injured enough to require mechanical ventilation in the first place. Optimizing these patients often must be done expeditiously, as many patients require emergent intubation or precipitously decline, though carefully considering a patient’s indication for ventilatory support as well as preparation based on their clinical situation will allow for a safe transition to mechanical ventilation. The intensivist should carefully and efficiently consider the patient’s neurologic, cardiovascular, pulmonary, gastrointestinal, and renal status prior to initiating ventilatory support.

MONITORING

Appropriate monitoring before, during, and after initiating invasive ventilation is essential. Continuous cardiac monitoring with frequent noninvasive blood pressure recording at least every 3 to 5 minutes should be performed in the peri-intubation period. Further invasive monitors can be helpful, but often the urgency of intubation precludes a delay in establishing further access. Patients where intubation is nonemergent and can be safely delayed, or those with extreme hemodynamic instability, may benefit from invasive arterial pressure monitoring, central access, and potentially continuous cardiac output monitoring prior to induction. Poor cardiac output and shock states result in significant peripheral SpO₂ lag compared to central arterial oxygenation. The delay is exacerbated by signal averaging of pulse oximetry and accentuated during hypoxia (i.e., starting at the inflection point of the oxyhemoglobin dissociation curve). The repercussion of this delay is that central arterial oxygenation can lag the peripheral SpO₂ monitor output for up to 60 to 90 seconds. This also results in a slow SpO₂ response after recovering from a desaturation episode such as with mask ventilation after a failed attempt. Forehead and ear probes are closer to the central circulation and respond more quickly than distal extremity probes. Forehead reflectance probes are often preferred in critically ill patients for this reason, and they provide more reliable signal detection during hypotension. Limited detection of cutaneous arterial pulsatility generally reduces accuracy of pulse oximetry with SBP <80 mm Hg.

Ensuring appropriate intravenous access prior to intubation is imperative. Initiating an intravenous line should be made a priority before preparing other interventions, though intubation should usually not be postponed for placement of a central line depending on a patient’s clinical status. If IV access cannot be quickly obtained in these patients, intraosseous access is appropriate. In patients with IV or central venous access already obtained, ensuring that the access is functional and consistent prior to intubation is important. Flushing IV lines, drawing back on a central line to ensure blood return, and evaluating for infiltration or questionable lines should be performed before any induction drugs are pushed, vasopressors started, or fluids bolused.

PRACTICAL APPROACH TO PHYSIOLOGIC OPTIMIZATION

Determining the urgency of intubation significantly contributes to the plan to optimize a patient prior. Unstable patients add complexity to the airway management strategy, and following the traditional “A-B-Cs” of resuscitation may contribute to deterioration. Emergent indications for ventilatory support such as acute aspiration and hypoxemia will not afford the intensivist the luxury of time to slowly optimize. Less urgent indications such as hypercapnia, secretion management, and upcoming procedures will usually provide more time. The intensivist should be mindful of the time constraints and prioritize life-saving maneuvers, and must understand what physiologic changes their interventions will produce to optimize patients appropriately. Physiologic changes during and immediately after intubation are broad, but oftentimes predictable (Table 18.1), and any clinician who can foresee what intubation and positive pressure will likely cause has an advantage of attenuating it beforehand. Prioritizing intubation versus preintubation resuscitation is a common clinical dilemma. Three main considerations may assist with the decision:

TABLE 18.1 Intubation Events and Effects

Intubation Events	Effects
Anxiety	Often patients are not wakeful, and their mental state is not contributing to physiologic changes. The need for intubation (or the cause of that need) may induce fear, anxiety, anger, or other normal responses which may cause the release of endogenous catecholamines. Other patients may be delirious at the time, and through their delirium have similar physiologic changes that will alter the appropriate course of action.²
Sedation and muscle relaxation	This intrinsic “will to live” is often uncovered on induction as it eliminates the catecholamine surge and patients can become quite hypotensive through changes in cardiac output or systemic vascular resistance. The effect is often worsened with positive pressure either through mask ventilation or by initiating mechanical ventilation.
Stimulation	Airway manipulation with laryngoscopy will often stimulate the release of endogenous epinephrine and commonly results in tachycardia, which may be the tipping point in patients who are already stressed with tachycardia and hypotension.
Positive pressure	Depending on a patient’s indication for intubation and their comorbidities, positive pressure ventilation can decrease preload, increase afterload, and alter pulmonary mechanics.³

Key Question: What is the reversibility and severity of the underlying physiology?

Acute decompensated heart failure with cardiogenic pulmonary edema from volume overload and hypertension often rapidly responds to aggressive medical therapy in minutes to hours, averting the need for intubation. However, acute heart failure from a ruptured papillary muscle and acute mitral regurgitation (MR) will not respond quickly and will likely need intubation to facilitate resuscitation and surgical repair. Both present with acute heart failure and pulmonary edema, but the treatment strategies and time course for each require a different airway management plan.

Similar situations exist with respiratory failure. Acute respiratory failure from exacerbations of asthma or chronic obstructive pulmonary disease (COPD) often responds relatively quickly to noninvasive respiratory support, and mechanical ventilation is generally delayed or avoided. Pneumonia or acute respiratory distress syndrome (ARDS), on the other hand, does not reverse rapidly and comes with a high noninvasive failure rate. Delaying intubation in patients with signs of failure or until refractory hypoxemia is associated with a high incidence of peri-intubation complications and adverse outcomes.

Key Question: What is the current cardiovascular status and risk of peri-intubation deterioration?

The cause of shock is an important consideration when deciding when and how to intubate. Positive pressure effects on cardiac function vary depending on the underlying cardiovascular state. Positive intrathoracic pressure reduces transmural cardiac pressure and left ventricular afterload, which may improve the performance of severe left ventricular dysfunction. Patients with normal or mildly reduced function or volume depletion, however, may deteriorate despite this because of reduced venous return from positive pressure. Prioritizing early resuscitation is important for these patients, especially those with prominent vasodilation (i.e., sepsis, cirrhosis, and anaphylaxis).
Mechanical ventilation can precipitate cardiovascular collapse in other forms of shock, however, such as right heart failure and pericardial tamponade. In these patients, delaying intubation to treat or attenuate the physiologic threat (e.g., pericardiocentesis) is prioritized.

Many critically ill patients present in compensated shock with a narrow pulse pressure but sustained normotension. Hypotension characterizing uncompensated shock is a late sign that develops when physiologic mechanisms are overwhelmed. As such, physiologic optimization of normotensive patients focuses on preventing pushing the patient into uncompensated shock, while in the hypotensive patient resuscitation should focus on restoring compensated shock to tolerate intubation. Normal or even elevated blood pressure should not be interpreted as a sign of safety with induction and is often a false sense of security. Shock index (SI = HR/SBP) helps identify vulnerable patients despite deceptively normal blood pressure. Elevated SI is associated with deterioration across a range of clinical conditions including intubation. Preintubation SI ≥0.8 independently predicts peri-intubation hemodynamic deterioration. However, one-third of patients develop peri-intubation despite an SI <0.8 and all critically ill patients should be respected as at risk.

Key Question: What is the anticipated clinical course?

In many critically ill patients, early resuscitation improves shock but patients may rapidly or slowly deteriorate after. Tissue edema from volume resuscitation or inflammation, progression of end-organ dysfunction, respiratory fatigue, and metabolic debt can all exhaust physiologic reserve during resuscitation. Thus, patients require frequent reassessment and close monitoring to decide the timing of intubation. Intubation should occur early when the downward cycle is identified, rather than wait for overt cardiovascular or respiratory failure.

Optimization by Organ System

One way to organize physiologic optimization is to consider separate organ systems and have specific interventions for each, informed by the underlying physiologic state as described in Chapters 6, 7, and 8. We suggest the following:

Neurologic

The neurologic system presents a double-edged sword with airway management. On the one hand, it is significantly stressed during the lead up to and initiation of positive pressure ventilation. Patients, if awake, are usually distressed from dyspnea or the sensation of impending airway compromise, often causing them to become hypertensive and tachycardic which can be detrimental to their perfusion depending on their premorbid condition and mask serious underlying hemodynamic problems. Second, inserting an endotracheal tube itself is stimulating as the tissues of the posterior oropharynx and larynx are incredibly sensitive due to their role in protecting the airway.⁴ Third, unexpected awareness during intubation is known to be incredibly distressing to patients and should always be avoided. On the other hand, the neurologic system, particularly in the brain-injured patient, is vulnerable to the hypotension that is often potentiated by the very induction agents used to protect the neurologic system. For the above reasons, it is critical to ensure an adequate and appropriate pharmacologic plan, whether topical anesthesia, or full induction, prior to intubating a patient in respiratory distress. There is no role for the old saying that “pain is the best pressor.”

Every patient requires some form of neurologic optimization. Some patients (e.g., those with unstable ischemic cardiomyopathy) may require mild sedation or antihypertensives prior to intubation to decrease the oxygen demand from the heart. Other patients (e.g., those with drug-induced psychosis or hypertensive crises) may require large doses of sedation or antihypertensives that risk dangerous respiratory suppression or induction-related hypotension.

Occasionally, patients may have such a tenuous cardiovascular status or hypoxemia refractory to preoxygenation that the consequences of induction are too great. In these patients, an awake technique with appropriate topicalization should be utilized (Chapter 16, Topical anesthetics and anesthesia for awake intubation). For most patients, however, some amount of sedating medications can be given (Chapter 12, Options) to decrease the risk of awareness, and when sedation is required the optimal strategy is RSI with full-dose induction agents (Chapters 13, Sedative agents for RSI and 14, Neuromuscular blocking agents).

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